The aim of study is to know the role of IgE in host defense to helminth infection. The study focused on the effect of IgE-level regulatory gene on the protection to helminth infection in mice. It has been demonstrated by myself that this gene regulates IgE production, restricted for IgE isotype and not restricted to antigens stimulated. this gene is considered to be equivalent to an atopy gene in humans. The strains of mice were divided into high and low responders under the regulation of this gene. the experiments were performed to determine IgE dependency of protection to helminths comparing between selective IgE-deficient and IgE-producing control mice of high or low IgE responder strains. Anti-helminth IgE antibody had protective roles in expulsion of Hymenolepis nana, resistance to Trichinella spiralis. IgE antibody dependency of protective immunity to Trichinellaspiralis was found only in the host expressing high IgE phenotype but not in low IgE phenotype. To clarify the effect of IgE-level regulatory gene on defense function to Trichinella spiralis, backcross (N2 generation) mice of high and low responders were infected with Trichinella spiralis. The half of N2 mice were high IgE responders and the other half were low responders, confirming my previous finding of one gene. IgE responsiveness in each of N2 mice was inversely correlated to the protective function to Trichinella spiralis. This result suggests that IgE-level regulatory gene regulates defense function to helminth as an IgE-dependent protection gene. Therefore, it would be likely that the fundamental role of IgE is protection to helminths.